I. Introduction

Myocardial infarctions are becoming increasingly common amongst younger adults. In fact, amongst patients in the Young-MI Registry, a retrospective cohort study that includes patients who suffered a myocardial infarction before 50 years of age at Massachusetts General and Brigham and Women’s Hospitals, one in five patients was age 40 years or younger. Additionally, the percentage of individuals who experienced a myocardial infarction at less than 40 years old between 2000 and 2016 increased by 1.7% annually.¹ Hyperlipidemia, type II diabetes, hypertension, smoking, abdominal obesity, psychosocial stress, alcohol consumption, and lack of fruit and vegetable consumption are among the known risk factors for a first MI, as demonstrated by the INTERHEART study conducted in 2004.² However, many patients without the aforementioned factors still suffer from MI’s, which suggests the presence of other elements contributing to increased MI risk.

Recent research has demonstrated that elevated levels of lipoprotein(a), or Lp(a), are associated with increased risk of developing coronary artery disease (CAD). A 2024 study, published in JAMA, analyzing coronary CT angiography scans of 299 patients found that those with a Lp(a) level of 125 nmol/L or higher had twice as much percent atheroma volume as patients with a Lp(a) level of less than 125 nmol/L.

When adjusted for other risk factors, every doubling of Lp(a) led to a 0.32% increase in percent atheroma volume of a period of ten years. In this study, higher Lp(a) levels were also associated with increased low-density, noncalcified plaque, as well as more pericoronary adipose tissue inflammation.³ A 2009 study, published in JAMA, analyzed the association between elevated Lp(a) and incidence of myocardial infarction, comprising of patients from the Copenhagen City Heart Study, the Copenhagen General Population Study, and the Copenhagen Ischemic Heart Disease study (40.486 patients in total), and found that elevated Lp(a) was associated with a hazard ratio of 1.22, indicating a causal link between elevated Lp(a) and increased risk of suffering from a myocardial infarction.⁴ A sample of 6,086 cases of first MI and 6,857 controls from the INTERHEART study was stratified by ethnicity and adjusted for age and sex, with the aim of determining whether there is an association between elevated Lp(a) level and incidence of first MI, and if this association holds true amongst individuals of varying ethnic backgrounds. The study showed that higher Lp(a) levels are associated with an increased risk of first MI, and that there is an especially large prevalence of elevated Lp(a) amongst patients from South Asia and Latin America.⁵

Apolipoprotein B (ApoB) is another emerging risk factor for CAD, and is a lipid carrier for chylomicrons, low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and very low-density lipoprotein (VLDL).⁶ ApoB is the glue that binds LDL to proteoglycans in the subendothelial space, allowing for LDL particle modification. This alteration of LDL particles promotes their retention as well as a vascular inflammatory response. Additionally, macrophages engulf these modified LDL particles, leading to foam cell formation and cell death. These dead cells as well as cholesterol crystals are a significant component of an atherosclerotic plaque’s necrotic core. In this manner, increased ApoB levels promote atherogenesis.⁷

This case focuses on a young, 29-year-old patient with moderately elevated LDL, history of type II diabetes and hypertension, and a normal Lp(a), who suffered from a myocardial infarction. Her ApoB was found to be elevated, suggesting this as a probable risk factor for her development of CAD. It is worth noting that traditional risk stratification tools do not include ApoB, and so this patient’s cardiac disease risk was underestimated.

II. Case Presentation

A 29-year-old South Asian female patient with past medical history of type II diabetes, hypertension, and hyperlipidemia presented with acute, severe, crushing, left-sided chest pain and dyspnea, as well as a syncopal episode. Family history is notable for death from myocardial infarction in her mother at the age of 47, as well as a maternal aunt who died prematurely from CAD (age unknown). Her only home medications were 1,000 mg of oral metformin taken twice per day and 15 units of injectable long-acting insulin glargine taken every night. On initial presentation, the patient’s heart rate was 88, blood pressure 140/113, respiratory rate 12, and O2 saturation 98% on room air. Her BMI was 24.26. Initial physical exam was unremarkable, with cardiovascular exam demonstrating 2+ bilateral radial, dorsalis pedis, and posterior tibial pulses, regular rate and rhythm, normal S1 and S2, no murmurs, rubs, or gallops, no lower extremity edema, and lungs that were clear to auscultation bilaterally. In the emergency room, her initial labs were notable for a troponin of 262 ng/L (normal≤ 14 ng/L), LDL of 147 mg/dL (normal<100 mg/dL), total cholesterol of 215 mg/dL (normal ≤200 mg/dL), HDL of 31 mg/dL (normal≧40 mg/dL), triglycerides of 373 mg/dL (normal ≤150 mg/dL), Hgb A1C of 14.3%, Lp(a) of 33.2 nmol/L (normal <75 nmol/L), Apolipoprotein A-1 of 116 mg/dL (normal 116-209 mg/dL), and ApoB of 152 mg/dL (normal <90 mg/dL). Her EKG on initial presentation showed normal sinus rhythm with normal axis, but was notable for T-wave flattening in V3-V6 and biphasic T waves in V2. There was no evidence of ST-segment elevation on EKG.

In the emergency room, the patient was given an aspirin load of 324 mg, heparin 3,950 units IV, 500 cc’s of normal saline, and sublingual nitroglycerin. Based on her significantly elevated troponin in the setting of crushing chest pain, with concerning EKG changes but without ST-segment elevation, a preliminary diagnosis of non-ST elevation myocardial infarction (NSTEMI) was made and the patient was taken to the cardiac catheterization laboratory for coronary angiography with possible stenting.

In the cardiac catheterization laboratory, the patient was found to have a total occlusion of the left circumflex coronary artery, as well as mild to moderate distal diffuse disease of the left anterior descending coronary artery. As demonstrated in Figure I, a balloon angiography was performed and a drug-eluting stent was placed in the left circumflex coronary artery, with resultant complete perfusion through the artery (TIMI 3 flow). After stent placement, the patient’s chest pain improved from a 10/10 to a 2/10. At the conclusion of the procedure, the patient was given ticagrelor and heparin, and taken to the Cardiac Care Unit (CCU).

Post-catheterization transthoracic echocardiogram demonstrated an ejection fraction of 55%, no wall motion abnormality, and grade I diastolic dysfunction. The patient was started on atorvastatin 80 mg daily, aspirin 81 mg daily, ticagrelor 90 mg twice per day, carvedilol 6.25 mg daily, and nitroglycerin 0.4 mg every five minutes as needed for chest pain. She was discharged from the hospital in stable condition two days after cardiac catheterization, with close cardiology follow-up.

Figure I:

Coronary angiography with percutaneous coronary intervention of the left circumflex coronary artery. (A) Angiogram showing 100% occlusion of left circumflex coronary artery. (B) Advancement of the guidewire. (C) Positioning of the stent. (D) Post-stenting TIMI-3 flow in the culprit vessel.